OBESITY

Group 5
What is obesity?

Obesity is defined as abnormal or

excessive fat accumulation that may
impair health. (WHO)
How do you classify
Obesity?
Body Mass Index (BMI) is a simple
index of weight-for-height that is
commonly used to classify
underweight, overweight and obesity in
adults.

It is defined as a person's weight in

kilograms divided by the square of his
height in meters (kg/m2).
 BMI classification
The International Classification of adult underweight, overweight and obesity according
to BMI
Classification BMI(kg/m )
2

Principal cut-off points Additional cut-off points

Underweight <18.50 <18.50

Severe thinness <16.00 <16.00

Moderate thinness 16.00 - 16.99 16.00 - 16.99

Mild thinness 17.00 - 18.49 17.00 - 18.49

18.50 - 22.99
Normal range 18.50 - 24.99
23.00 - 24.99

Overweight 25.00 25.00

25.00 - 27.49
Pre-obese 25.00 - 29.99
27.50 - 29.99
Obese 30.00 30.00
30.00 - 32.49
Obese class I 30.00 - 34.99
32.50 - 34.99
35.00 - 37.49
Obese class II 35.00 - 39.99
37.50 - 39.99

Obese class III 40.00 40.00

Source: Adapted from WHO, 1995, WHO, 2000 and WHO

Adults

For adults, WHO defines obesity as follows:

Obesity is a BMI greater than or equal to 30.

BMI provides the most useful population-level

measure of obesity as it is the same for both
sexes and for all ages of adults. However, it
should be considered a rough guide because it
may not correspond to the same degree of
fatness in different individuals.
Children under 5 years
of age
For children under 5 years of age:
obesity is weight-for-height greater than 3
standard deviations above the WHO Child
Growth Standards median.
Children aged between 5
19 years
Obesity is defined as follows for children aged
between 519 years:
obesity is greater than 2 standard
deviations above the WHO Growth
Reference median.
What causes obesity?

The fundamental cause of obesity and overweight

is an energy imbalance between calories
consumed and calories expended. Globally, there
has been:

an increased intake of energy-dense foods that are

high in fat; and

an increase in physical inactivity due to the

increasingly sedentary nature of many forms of
work, changing modes of transportation, and
increasing urbanization.
Regulation of food intake
and energy storage
Stability of the bodys total mass and composition
over long periods requires that energy intake
match energy expenditure.
 The hypothalamus
contains hunger and
satiety centers
Lateral nuclei of the hypothalamus
Feeding center
Stimulation causes an animal to eat voraciously
(hyperphagia)

Ventromedial nuclei of the hypothalamus

Satiety center
Sense of nutritional satisfaction that inhibits the
feeding center
Aphagia even in the presence of appetizing food
Destruction causes voracious and continued eating
-> Obesity
 The hypothalamus
contains hunger and
satiety centers
Paraventricular, dorsomedial and arcuate
nuclei
Lesions of the paraventricular nuclei cause excessive
eating
Lesions of the dorsomedial nuclei usually depress
eating behavior
 Neurons and
neurotransmitters in the
hypothalamus that stimulate
or inhibit feeding
2 types of neurons in the arcuate nuclei of the
hypothalamus for appetite and energy
expenditure

Pro-opiomelanocortin (POMC)
Produce -melanocyte-stimulating hormone (-
MSH), cocaine- and amphetamine-related transcript
(CART)

Neuropeptide Y (NPY) and agouti-related

protein (AGRP)
Produce orexigenic substances
 Neurons and
neurotransmitters in the
hypothalamus that stimulate
or inhibit feeding
Pro-opiomelanocortin (POMC)
Decrease food intake
Increase energy expenditure

Neuropeptide Y (NPY) and agouti-

related protein (AGRP)
Increase food intake
Decrease energy expenditure
 Neurons and
neurotransmitters in the
hypothalamus that stimulate
or inhibit feeding
Pro-opiomelanocortin (POMC)
Release -MSH
Acts on melanocortin receptors on the
paraventricular nuclei
MCR-3 and MCR-4 = reduces food intake
and increases
energy expenditure
 Neurons and
neurotransmitters in the
hypothalamus that stimulate
or inhibit feeding
MCR-4 mutations
Extreme obesity

Excessive activation of melanocortin system

Reduces appetite

Agouti-related protein (AGRP)

Natural antagonist of MCR-3 and MCR-4
Increases feeding by inhibiting effects of -MSH to
stimulate melanocortin receptors
 Neurons and
neurotransmitters in the
hypothalamus that stimulate
or inhibit feeding
Neuropeptide Y (NPY)
When energy stores of the body are low, orexigenic
neurons are activated to release NPY
Stimulates appetite
Reduced firing of POMC
Decrease activity of the melanocortin pathway,
stimulating appetite
 Factors that regulate
quantity of food intake
Short-term regulation
Prevent overeating

Long-term regulation
Maintenance of normal quantities of
energy stores
in the body
Short-term regulation of food
intake
GI filling inhibits feeding

Distention of stomach and duodenum

reduces
desire for food

Stretch inhibitory signals transmitted to

suppress
feeding centers
Short-term regulation of food
intake
GI hormonal factors suppress feeding
Cholecystokinin (CCK)
Released in response to fat and proteins
entering the duodenum
Satiation and meal cessation
Only prevents overeating during meals
Peptide YY (PYY)
Secreted from the entire GI tract, especially
from the ileum and colon
Food intake stimulates PYY release
Influenced by amount and composition of
food (high fat content)
Short-term regulation of food
intake
GI hormonal factors suppress feeding
Glucagon-like peptide (GLP)
Secreted in the presence of food in the
intestines
Enhances glucose-dependent insulin production

and secretion from the pancreas

GLP and insulin both tend to suppress appetite
Short-term regulation of food
intake
Ghrelin increases feeding

Ghrelin is released by the oxyntic cells of the

stomach and by the intestine

Blood levels rise during fasting and peak just

before eating, and fall rapidly after a meal
Short-term regulation of food
intake
Effect of concentrations of glucose, amino acids
and lipids on hunger and feeding

Decrease in blood glucose and lipids (ketoacids) causes hunger

A rise in blood glucose level increases the rate of firing of glucoreceptor

neurons in the satiety center in the ventromedial and paraventricular nuclei of
the hypothalamus

The same increase in blood glucose level simultaneously decreases the firing
of glucosensitive neurons in the hunger center of the lateral hypothalamus
Short-term regulation of food
intake
Feedback signals from adipose tissue regulate
food intake
Most of the stored energy in the body consists of fat

The hypothalamus senses energy storage through the actions of leptin

Released from adipocytes

When the amount of adipose tissue increases,

leptin production is also increased
Short-term regulation of food
intake
Feedback signals from adipose tissue regulate
food intake
Leptin circulates to the brain and occupies leptin receptors in the
hypothalamus
POMC and AGRP/NPY neurons of the arcuate nuclei
Neurons of the paraventricular nuclei

Has multiple actions that decrease fat storage

Decrease production of appetite stimulators NPY and AGRP
Activation of POMC neurons
Activation of melanocortin receptors
Short-term regulation of food
intake
Feedback signals from adipose tissue regulate
food intake
Increased production of corticotropin-releasing hormone (CRH) which
decreases food intake

Increase Sympathetic nerve activity

Increase metabolic rate and energy expenditure

Decrease Insulin secretion

Decrease energy storage
Short-term regulation of food
intake
Feedback signals from adipose tissue regulate
food intake
Leptin and leptin receptor mutations
Hyperphagia and morbid obesity
*plasma leptin levels increase with increasing obesity

Leptin resistance
Signaling pathways resistant to activation by leptin in obese people
Continue to eat despite high levels of leptin
 Long-term regulation

When the energy stores of the body fall below normal,

feeding centers in the hypothalamus become active
Hunger

With abundant energy (fat stores), sensation of hunger

is lost
Satiety
What are common health
consequences of obesity?
Raised BMI is a major risk factor for
noncommunicable diseases such as:
cardiovascular diseases (mainly heart disease and
stroke), which were the leading cause of death in
2012;

diabetes;

musculoskeletal disorders (especially osteoarthritis

a highly disabling degenerative disease of the
joints);

some cancers (including endometrial, breast,

ovarian, prostate, liver, gallbladder, kidney, and
colon).
Treatment and
Management
Treatment of obesity starts with
comprehensive lifestyle management
(ie, diet, physical activity, behavior
modification), which should include the
following:
Self-monitoring of caloric intake and
physical activity
Goal setting
Stimulus control
Nonfood rewards
Relapse prevention
Treatment and
Management
Treatment of obesity starts with
comprehensive lifestyle management
(ie, diet, physical activity, behavior
modification), which should include the
following:
Self-monitoring of caloric intake and
physical activity
Goal setting
Stimulus control
Nonfood rewards
Relapse prevention
Pharmacologic therapy
Currently, the 3 major groups of drugs used
to manage obesity are as follows:
Centrally acting medications that impair dietary
intake
Medications that act peripherally to impair dietary
absorption
Medications that increase energy expenditure
THANK YOU!